Metal silver is widely used in our daily life and in medical care.Silver Nanoparticle Due to the breakthrough of nanotechnology, nano silver particles (hereinafter referred to as AgNPs) have gained more benefits. However, the increase in the use of AgNPs in various fields inevitably leads to an increase in the potential risk of nanoscale particles, which raise concerns about environmental safety and human health. In recent years, Silver Nanoparticle researchers have evaluated the toxicities of AgNPs and sought to explore their cellular and molecular toxicity mechanisms.
Once AgNPs enter the body, some may remain in the original target tissue, but in principle they will be transported through the bloodstream or lymphatic system, Silver Nanoparticle distributed to the body's secondary target organ, causing a specific organ or systemic response. In rodents, AgNPs, given oral, intravenous, or intraperitoneal injection, have demonstrated that the brain, liver, spleen, kidney, Silver Nanoparticle and testis are predominantly secondary target organs throughout the body. Such organ distribution patterns suggest that the potential toxicity of AgNPs can cause neurotoxicity, immunotoxicity, nephrotoxicity, and reproductive toxicity in vivo.
Cytotoxicity, such as reactive oxygen species, Silver Nanoparticle DNA damage, changes in intracellular enzyme activity, and the occurrence of apoptosis and necrosis, have been associated with liver toxicity induced by AgNPs in vivo. Basically, when the cells are facing unfavorable conditions, Silver Nanoparticle several steady-state processes will begin to sustain cell survival, one of which is autophagy.Silver Nanoparticle Autophagy can act as a cell defense process that is essential to counteract the toxicity of AgNPs, but does not maintain autophagic activity, accompanied by reduced energy, may contribute to the occurrence of apoptosis and subsequent liver function damage
"Autophonic tide" is used to express the autophagy after the dynamic process, first of all the formation and maturation of autophagosomes, followed by autophagylosin fusion, Silver Nanoparticle and finally hydrolyzed vesicle wrapped cell components and the release of macromolecules Cytoplasm. In this regard, any of the above steps in the process of interruption as cell autophagy tide is flawed. AgNPs exposure increased LC3-I to LC3-II in a dose-dependent manner, and the accumulation of p62 protein was dose-dependent. Silver Nanoparticle This suggests that although AgNPs activate autophagy, they eventually lead to autophonic tide being blocked. In addition to the problem of autophagy dysfunction, RNP and apoptosis were also increased after AgNPs exposure.
More and more evidence suggests that post-translational modifications, Silver Nanoparticle especially phosphorylation, acetylation, and ubiquitination, determine the activity and / or aggregation of proteins involved in performing autophagy and fine-tuning autophagous tide development. Silver Nanoparticle Increased cellular stress can lead to the collapse of the post-translational modification system or cause nonspecific modification that does not occur under physiological conditions.
Ubiquitination has long been considered the key to controlling the fate of proteins, which is the process of labeling proteins to be degraded by proteasomes. More recently, Silver Nanoparticle there is growing evidence that conjugated ubiquitin chains determine autophagy selectivity.